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Defense response signaling for disease resistance in rice




Bruce, Myron Anthony, author
Leach, Jan E., advisor
Chisholm, Stephen, committee member
Ranu, Rajinder, committee member
Bush, Daniel R., committee member

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Plant disease resistance is often associated with a type of programmed cell death (PCD) called the hypersensitive response (HR). Upon recognition of pathogen proteins or their activity, the affected cell and surrounding cells commit to the HR to limit pathogen spread throughout the plant. This mechanism of plant disease resistance renders a pathogen avirulent on the host plant. Lesion mimics (LM) are a class of mutant or transgenic plants that spontaneously show lesions resembling the HR in the absence of biotic stress. Based on the association of the LM phenotype to cell death and its similarity to disease symptoms and the HR, this phenotype is a useful tool to dissect and understand the plant defense response. To identify genes that when mutated result in the LM phenotype in rice, we used a microarray approach. By hybridizing labeled genomic DNA from an allelic series of deletion mutants to an oligonucleotide microarray, we identified candidate genes and genic regions that were deleted in a set of mutants. For one mutant, spl1, mutations in a cytochrome P450 gene were confirmed to confer the LM phenotype. A genome browser developed to handle these microarray data is a community resource that enables researchers to rapidly identify untagged deletion mutations in rice. Members of the 14-3-3 protein family were recently shown to be positive regulators of cell death and the HR in Arabidopsis. In contrast, the work herein shows that a rice 14-3-3 protein is a negative regulator of cell death and resistance. Transgenic plants carrying a construct that silences the rice 14-3-3 gene GF14e exhibit a LM phenotype and enhanced resistance to two distinct rice pathogens, Xanthomonas oryzae pv. oryzae and Rhizoctonia solani. These GF14e-silenced plants also showed enhanced expression of genes associated with salicylic acid (SA) mediated defense responses, including members of the peroxidase gene family. The GF14e-silenced plants did not show enhanced expression of marker genes associated with the ethylene response pathway, indicating that GF14e may negatively regulate SA mediated defense responses, but does not affect ethylene regulated responses. Silencing GF14e results in the up regulation of several defense responsive peroxidases. cDNA from GF14e silenced plants was used in quantitative PCR (qPCR) to assay expression of four peroxidase genes. Of these, three showed significant upregulation in 2 weeks after sowing (WAS) and 5 WAS GF14e-silenced plants. The promoters of the three upregulated genes (PO-C1, Pox8.1, Pox22.3) contain at least one W-box element. In contrast, the peroxidase (Pox5.1) that did not show upregulation and is not upregulated in R gene mediated responses had no W-box elements. W-box elements are binding sites for the WRKY class of transcription factors. This result, coupled with bioinformatic predictions of potential rice 14-3-3 clients, and the observation that some WRKY genes are upregulated in GF14e silenced lines indicates that GF14e may negatively regulate WRKY transcription factors related to cell death and defense responses. Based on the implication that one 14-3-3 protein negatively regulates defense responses related cell death, provides a framework to develop a model for how this protein might function in the plant disease resistance response.


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lesion mimic


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